Mammalian outer hair cells (OHC's) can change length at acoustic frequencies when they are electrically stimulated. Recently we have suggested that these length changes are driven by a novel force generator mechanism embedded in the lateral plasma membrane. The performance of this force generator mechanism embedded in the lateral plasma membrane. The performance of this force generation mechanism is dependent on the cell turgor, suggesting that water transport and cell volume regulation are critical processes for OHC's physiology. We have observed that OHC electromotility is inhibited by pCMPS. PCMPS is known to inhibit water transport in different cell populations by targeting SH-groups in the transmembrane aqueous channels of anion and water transporting proteins. To verify if any if these channel proteins are present in OHC's we have raised polyclonal antibodies against synthetic peptides corresponding to conserved regions in anion exchanger (AE) protein family, and the major intrinsic protein (MIP) family responsible for water transport. The anti- AE antibody recognized a single band of approximately 140 Kda on Western Blots of guinea pig cochlea, and by immunofluorescence it labeled OHCs. The second antibody, raised against the MIP protein family, recognized a single band of approximately 45 Kda on Western Blots of brain and cochlea. This antibody labelled inner Hair Cells, Deiter's and Hensen's cells but not OHCs. We conclude that members of both protein families are present in the guinea pig organ of Corti, and AE-like proteins may be involved in OHC electromotility. OHC shape is maintained by a cross-linked lattice of circumferential filaments beneath the lateral plasma membrane. Structural studies showed that the cross links are 70-80nm long and that the lattice is stiffer circumferentially than it is longitudinally. Analysis of the orientation of circumferential filaments showed that the lattice is composed of discrete domains of up to 10 um2. Relative movements domains could allow changes of cell shape without disrupting the unit structure of the lattice, thus allowing the cell cortex to retain its elastic responses to high- frequency deformations.